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Exposure of the lung to carbonaceous nanoparticles: single walled carbon nanotubes (SWCNT) leads to the development of pulmonary fibrosis (PF) and induction of a network of pro-fibrotic/pro-inflammatory cytokines including TGF-beta1 and osteopontin (OPN). TGF-beta1 is involved in fibrotic remodeling including fibroblast differentiation and enhanced deposition of collagen in the extracellular matrix. As part of the inflammatory cascade, OPN acts as a chemoattractant to guide polymorphonuclear neutrophils (PMN) and macrophages (M Phi) to the area of insult/injury and is also involved in collagen deposition. Potential interactions between OPN and TGF-beta1 have not been investigated even though both cytokines have been shown to be upregulated in response to SWCNT. We hypothesize that OPN increase in response to SWCNT potentiate TGF-beta1 production in lung cells. To test our hypothesis two cell types, alveolar epithelial cells (MLE-15) and RAW 264.7 M Phi were treated with SWCNT (6 mu g/cm2 - 48 mu g/cm2, for 24 hours). Exposure of the cells to SWCNT resulted in significantly enhanced OPN released found in the incubation medium (39.1% for MLE-15 and 38.6% for RAW 264.7 M Phi vs. respective controls). Using an OPN antibody we demonstrated an inhibition of OPN production in response to SWCNT. Further studies are needed to evaluate interplay between OPN and TGF-beta1 and their role in SWCNT induced pulmonary fibrosis.